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Int Immunopharmacol ; 31: 195-9, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26745713

RESUMO

If apoptotic cells are not removed efficiently, they may proceed to the stage of secondary necrosis, which would cause inflammation. Therefore, identification of cause(s) and agent(s) for down-modulating phagocytosis of apoptotic cells would help understand the pathologies. In this study we found that macrophage-mediated phagocytosis of apoptotic cells was suppressed by both soluble and particulate ß-glucan. This suppression was not observed when secondary necrotic cells were used. The adhesion of apoptotic cells to macrophages was not suppressed by soluble ß-glucan, suggesting that soluble ß-glucan suppresses phagocytosis at a post-adhesion step. Experiments involving PKC inhibitors suggested that PKC-ßII is required for phagocytosis of apoptotic cells but not secondary necrotic ones by macrophages. Translocation of GFP-PKC-ßII from the cytoplasm to membranes occurred upon interaction with apoptotic cells but not secondary necrotic ones. Such translocation was inhibited by soluble ß-glucan. Overall, this study suggests that suppression of macrophage-mediated phagocytosis of apoptotic cells by soluble ß-glucan is due to a failure of PKC-ßII translocation.


Assuntos
Membrana Celular/metabolismo , Citoplasma/metabolismo , Macrófagos/efeitos dos fármacos , Fagocitose/efeitos dos fármacos , Proteína Quinase C beta/metabolismo , Transporte Proteico/efeitos dos fármacos , beta-Glucanas/farmacologia , Animais , Apoptose , Células Cultivadas , Macrófagos/fisiologia , Camundongos , Camundongos Endogâmicos ICR
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